Coronary

Artery

Disease

Dr. Amitesh Aggarwal 1

Ebers papyrus, ca. 1555 BCE

Ebbell B, The Papyrus Ebers: The greatest Egyptian medical document. 1937,

Copenhagen, Levin and Munkfgaard

“If thou examinist a man for

illness in his cardia, and he

has pains in his arms, in his

breasts and on one side of

his cardia...it is death

threatening him.”

2

Coronary anatomy

3

Spectrum of CAD

CAD / IHD Stable

Angina

ACS

UA

NSTEMI

STEMI

Asymptomatic

(subclinical)

ICMP

SCD

4

CAD Coronary Artery Disease

IHD Ischemic Heart Disease

Condition in which there is an inadequate

supply of blood and oxygen to a portion of

the myocardium;

Most common cause is atherosclerotic

disease of an epicardial coronary artery

sufficient to cause a regional reduction in

myocardial blood flow and inadequate

perfusion of the myocardium.

5

Angina

Discomfort in the chest or adjacent areas

caused by myocardial ischemia but

without myocardial necrosis.

(a) retrosternal pressure, pain, discomfort,

or heaviness that

(b) radiates to the neck, jaw, left arm, or

shoulder,

(c) precipitated by exertion and relieved by

rest or nitroglycerin, lasting <10 minutes.

6

ACS

Spectrum of clinical presentations ranging from those for STEMI to presentations found in NSTEMI or in UA.

In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery.

7

Unstable Angina

Angina pectoris or equivalent ischemic

discomfort with at least one of three

features:

(1) it occurs at rest (or with minimal exertion),

usually lasting >10 min;

(2) it is severe and of new onset (i.e., within the

prior 4–6 weeks); and/or

(3) it occurs with a crescendo pattern (i.e.,

distinctly more severe, prolonged, or

frequent than previously) 8

NSTEMI

Clinical features of UA

+

Evidence of myocardial necrosis

(elevated cardiac biomarkers)

+

absence of persistent ST elevation

9

STEMI

WHO DEFINITION (1994)

Two out of three criteria

Symptoms (chest pain > 20 minutes )

ECG

Bio-markers (CK MB, Trop T/I)

10

Universal Definition of Myocardial Infarction

(2007)

Type 1;Type 2;Type 3;Type 4a;Type 4b;Type 5

11

Spontaneous MI related to ischaemia due to primary

coronary event such as plaque erosion & / or rupture

It identifies MI due to atherosclerotic coronary arterial

occlusion only

Clinical Classification of MI

Type 1

Rise and/or fall of cardiac biomarkers (preferably

troponin) above URL with evidence of at least 1 of the

following :

* Symptoms of ischemia

* ECG changes indicative of new ischemia

* Development of pathological Q waves

* Imaging evidence of new loss of viable

myocardium or new regional wall motion abnormality 12

ECG changes in AMI (In absence of LVH & LBBB)

ST elevation

– New ST elevation at the J-point in two contiguous leads with the cut-off points: >0.2 mV in men or > 0.15 mV in women in leads V2-V3 and/or >0.1 mV in other leads

ST depression &/or T-wave changes

– New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads ; and/or T inversion >0.1 mVin two contiguous leads with prominent R-wave or R/S ratio >1

New LBBB

Development of Q-waves 13

ECG changes in AMI (In absence of LVH & LBBB)

Hyper- acute T wave amplitude with prominent symmetrical T-wave in at least two contiguous leads is earliest manifestation of AMI

ST segment equivalent – ST depression in V1-V3 with terminally positive T-wave with reciprocal ST elevation in V7-9

Pseudonormalisation of previously inverted T-waves

14

Clinical Classification of MI

Type 2

MI secondary to ischaemia due to either O2 demand or decreased supply, eg, coronary artery spasm, coronary embolism, anemia, arrhythmias, HTN or Hypotension

There is no coronary artery occlusion

No scope of reperfusion therapy & antithrombotics

15

Sudden unexpected cardiac death, including

cardiac arrest, often with symptoms suggestive

of myocardial ischaemia, accompanied by

presumably new STelevation, or new LBBB, or

evidence of fresh thrombus in a coronary artery

by angiography and/or at autopsy, but death

occurring before blood samples could be

obtained, or at a time before the appearance of

cardiac biomarkers in the blood

Clinical Classification of MI

Type 3

16

Myocardial infarction associated with PCI

– Embolisation of clot or debris

– Slow flow or no reflow

– Dissection

– Side branch stenosis

– Disruption of collaterals

(increases > 3X URL of biomarker)

Type 4b MI associated with stent thrombosis as documented

by angiography or at autopsy

Clinical Classification of MI

Type 4a

17

Myocardial infarction associated with CABG

Biomarker > 5 X of URL during first 72 h

following CABG, when associated with the

appearance of new pathological Q-waves or

new LBBB, or angiographically documented

new graft or native coronary artery occlusion,

or imaging evidence of new loss of viable

myocardium

Clinical Classification of MI

Type 5

18

Epidemiology

Modified,

WHO 2002

19

20

Mortality rates for CAD in Asian Indians in different countries

21

• Median age of first heart attack is 53 years

• Incidence of CAD in young Indians is 14%–16%

• Mortality attributable expected to rise by 113%

in men and 94% in women from 1985 to 2015

• Indian risk of CAD is 3-4 X White Americans 6

X Chinese 20 X Japanese.

• Manifests a decade earlier in ethnic Indians.

• Prevalence Urban (10.5 %) vs. Rural (4.5 %)

• Prevalence Men (7.4 %) vs. Women (4.5 %)

Indian Scenario

22

Coronary Artery Disease Other than

Atherosclerosis

Arteritis Takayasu disease

Trauma Laceration, Radiation

Coronary mural thickening Homocysteinuria

Luminal narrowing Spasm (Prinzmetal angina)

Emboli Infective endocarditis

Congenital Anomalies ALCAPA

O2 Demand-Supply Disproportion AS

Miscellaneous Cocaine abuse

23

RISK FACTORS OF ATEROSCLEROSIS

Age

Sex

Menopause

Family history of DM, HTN, IHD etc.

Genetic profile

Vascular anomaly (ostial obstruction)

Homocysteine

Fibrinogen

Lipoprotein ‘a’

Markers of Fibrinolytic function

Markers of Inflammation (hs – CRP, IL – 6, PAI)

Non modifiable Modifiable

Novel Atherosclerosis Risk factors

Smoking

Hypertension

Dyslipidemia

Diabetes

Insulin resistance

Exercise/Obesity

Sedentary life style

Mental Stress

Estrogen status

Cocaine use

Abnormal lipids, smoking, hypertension,

diabetes, abdominal obesity, psychosocial

factors, consumption of fruits & vegetables,

alcohol and regular physical activity account for

most of the risk of MI worldwide in both sexes

and at all ages in all regions

25

• Each of these factors significantly increases the risk of CAD

• When these factors combine in single individual, their effects

become multiplicative

Smoking Dyslipidemia

Hypertension

26

Vascular Atherosclerosis is an ongoing process

from day of creation to day of destruction

Fatty streak Transitional plaque Mature plaque Ruptured plaque

with thrombus

formation

Thrombus Extra cellular lipid pool

Foam cells Smooth muscle cells

Fibrous cap

Evolution of Atherosclerotic Plaque

28

Pathophysiology of Stable

and Unstable Plaques

Unstable plaque

Stable plaque

Thin fibrous cap

Thrombus

Thick fibrous cap

Smooth muscle cells

Lipid rich core and

macrophages

Media

29

Naghavi et al. Circulation. 2003;108:1664

Non-Stenotic Vulnerable Plaques overall are More Dangerous Since

they are far More Frequent than Stenotic Ones

Plaque remodeling

31

Angina

Discomfort in the chest or adjacent areas

(a) retrosternal pressure, pain, discomfort,

or heaviness that

(b) radiates to the neck, jaw, left arm, or

shoulder,

(c) precipitated by exertion, emotional

stress, medical or surgical illness, morning

and relieved by rest or nitroglycerin,

lasting <10 minutes.

32

33

Anginal equivalents

Dyspnea without pain

Atypical location of the pain – epigastric

Apprehension and nervousness

Sudden mania or psychosis

Syncope

Profound weakness

Acute indigestion 34

Unstable Angina/ NSTEMI

Angina pectoris or equivalent ischemic

discomfort with at least one of three

features:

(1) it occurs at rest (or with minimal exertion),

usually lasting >10 min;

(2) it is severe and of new onset (i.e., within the

prior 4–6 weeks); and/or

(3) it occurs with a crescendo pattern (i.e.,

distinctly more severe, prolonged, or

frequent than previously) 35

STEMI

• Angina pectoris or equivalent ischemic

discomfort

• May be accompanied by weakness,

vomiting, sweating, dizziness, palpitations,

cold perspiration, and sense of impending

doom

• Pronounced circadian periodicity for the time

of onset of STEMI, with peak incidence of

events between 6 AM and 12 noon

36

Atypical presentations of STEMI

heart failure - dyspnea without pain

classic angina pectoris without severe or prolonged episode

atypical location of the pain

central nervous system manifestations

apprehension and nervousness

sudden mania or psychosis

Syncope

overwhelming weakness

acute indigestion

peripheral embolization

37

MI patients without chest discomfort

More likely to be

Older

Women

Diabetic and/or have prior heart failure

Delayed longer before they went to the

hospital

Less likely to be diagnosed as having an MI

when admitted

Less likely to receive fibrinolysis or primary PCI,

aspirin, beta-blockers or heparin

2.2 times more likely to die during the

hospitalization

38

ANGINA / MI WITH NORMAL

CORONARY ARTERIES

Seen in 6% of pt.

More common in women (mechanism difficult to establish)

Tend to be young and have relatively few coronary risk

factors, except smoking.

Usually no history of angina pectoris prior to the infarction.

The infarction in these patients is usually not preceded by

any prodrome,

clinical, laboratory, and ECG features of STEMI are

otherwise indistinguishable from classical STEMI

In patients who recover, areas of localized dyskinesis and

hypokinesis can often be demonstrated by left ventricular

angiography. 39

PHYSICAL EXAMINATION Frequently negative

But careful search for

Valve disease (aortic valve)

Left ventricular dysfunction

(cardiomegaly , gallop rhythm)

Manifestation of arterial diseases

(carotid bruits peripheral vascular

diseases)

Unrelated condition that exacerbate

angina (anemia, thyrotoxicosis) 40

Findings & Implications in MI

CVS

• General: Restless, agitated, Levine’s sign

• Skin: Cool, clammy, pale, ashen

• Low-grade fever: response to myocardial necrosis

• Hypertension, tachycardia: sympathetic tone

(AWMI)

• Hypotension, bradycardia: vagal tone (I/P MI)

• Small-volume pulses: Low cardiac output

• Irregular pulse: Atrial / vent arrhythmias, CHB

• Paradoxical “ectopic” systolic impulse: LV

dyskinesis, ventricular aneurysm (AWMI)

41

Findings & Implications in MI

• Soft S1: LV contractility; 1° AV block (IW MI)

• S4 gallop: LV compliance

• Paradoxically split S2: Severe LV dys, LBBB

• S3 gallop, pulmonary rales, pulsus alternans:

LV systolic dys (CHF >25% of myocardium)

• JVP, Kussmaul’s sign, hypotension, RV S4

and S3 gallops, clear lungs: RVMI

• Pericardial friction rub: Pericarditis

• Absent pulses and murmur of AR: Aortic

dissection

CHEST

May be normal or few basal crackles: Pulmonary

congestion

42

EVALUATION

Asymptomatic

LAB IMAGING ED

Symptomatic

LAB IMAGING

43

RISK FACTORS

Blood Suger

Serum Lipids

hs-CRP

Homocysteine

Fibrinogen

Lipoprotein (a)

44

Biomarkers in CAD

Pro inflammatory markers. IL-1B, IL-6, TNF-alpha

Antiinflammatory cytokines IL-4. IL-6

Soluble cytokines receptors/antagonists

SIL-6, STNF, SIL

Cellular adhesion molecules sIAM-1, SVCAM, SEs, Ps

Matrix degradation enzymes mMP-3,9

Endothelium sICAM, P Selectin

Inflammation CRP, ALB, FBN, LC, SAA

CAD

45

Prognosis with Biomarkers

Relative risks of future myocardial infarction among apparently healthy men

46

Imaging

combination of tests to

diagnose the extent

and spread of

atherosclerosis

ABI

Stress testing

CIMT

CTA

Doppler study

IVUS

MRA

Angiography

CCS

47

Ankle Brachial Index This index is ratio of SBP measured at ankle to

SBP measured at brachial artery

Normal ABI should be ≥ 1.0

48

Flow Mediated Dilatation Early assessment of atherosclerosis

Endothelial dysfunction is considered to be the first stage

of atherosclerosis.

Determining efficacy of treatment

Cuff is inflated to 50 mm Hg above subject’s resting

systolic pressure and remains inflated for 4 min. The cuff is

then deflated and the 2-min image data are acquired

49

CIMT Carotid IMT measurement is

a viable predictor of the

presence of coronary

atherosclerosis and its clinical

sequelae

50

Exercise ECG / TMT to assess patients with suspected or proven

cardiovascular disease

to estimate prognosis and to determine functional

capacity, the likelihood and extent of CAD and the

effects of therapy.

In lead V4 , the TMT is abnormal early in the

test, reaching 0.3 mV (3 mm) of horizontal ST

segment depression at the end of exercise.

The ischemic changes persist for at least 1

minute and 30 seconds into the recovery

phase. This type is consistent with a severe

ischemic response. 51

MYOCARDIAL PERFUSION

SCANNING

Helpful in pt with uninterpretable exercise test

Accuracy higher than exercise ECG

scintiscan of myocardium at rest and during stress

after iv radioactive isotopes thallium.

If Perfusion defect present during stress but not

rest -reversible myocardial ischemia

Persistence perfusion defect during both phase

-previous MI 52

Patient with reversible perfusion defect in the inferior and anterior

wall and an irreversible perfusion defect in the septum

53

Coronary calcium Scoring

quantitatively assess coronary calcium using

Agatston CCS

surrogate for plaque burden

shown to provide powerful prognostic information

absence of coronary calcium (CCS 0), while not

excluding the presence of noncalcified plaque,

virtually excludes significant coronary

atherosclerosis

54

Significant Coronary Artery Calcium (Score >400)

55

IVUS Advantage

– Vessel wall + lumen visualization

– Plaque characterization

Disadvantage

– Need to instrument vessels

– Limited to proximal segments

– Not as well validated for clinical decision making

Atheroma

Potentially unstable

Echolucent

56

3.1 mm

3.1 mm

Angiography Fails to Depict

Coronary Arterial Remodeling

57

Symptomatic

• Serum biomarkers for cardiac damage

• Serum lipids

• Blood sugar

• ECG

• Echo

• Myocardial perfusion scans

• CTA/ MRA

• CAG

58

post-acute MI and Biomarkers

Normal - UA Increased - NSTEMI / STEMI

Should be measured at 0hrs, 6-9hrs, 12-24 hrs after admission 59

Biomarker Range of Times

to Initial

Elevation, h

Mean Time to

Peak Elevations

(Nonreperfused)

Time to

Return to

Normal

Range

CK-MB 3-12 h 24 h 48-72 h

cTnI 3-12 h 24 h 7-10 d

cTnT 3-12 h 12 h–2 d 7-14 d

Myoglobin 1-4 h 6-7 h 24 h

Biomarkers of Cardiac Damage

60

CK-MB

•Rapid, cost-

efficient, accurate

assays

•Ability to detect

early reinfarction

•Lack of specificity

with skeletal

muscle

disease/injury

•Low sensitivity

during early MI (<6

h) or late (>36 h)

after symptom

onset and for

minor myocardial

damage

Myoglobin

•High sensitivity

•Useful in early

detection of MI

•Detection of

reperfusion

•Most useful in

ruling out MI

•Very low

specificity with

skeletal muscle

injury or disease

•Rapid return to

normal

Troponins

•Greater

sensitivity and

specificity than

CK-MB

•Detection of

recent MI up to 2

weeks after

onset

•Detection of

reperfusion

61

ECG

Classic changes of necrosis (Q waves), injury (ST elevation), and ischemia

(T wave inversion)

In recovery, the ST segment is earliest change to normalizes, then T wave;

the Q wave usually persists for years after infarction

62

Hyperacute T Waves (over 50% of preceding R)

ST-T elevation (>1mm in limb or precordial

leads)

ST depression in Lead V1, Lead V2 (Posterior

MI)

T Wave inversion

Q Waves (.04 sec and 1/3 height of R Wave)

New left ventricular strain pattern

New Left Bundle Branch Block

63

Sequence of ECG Changes

64

65

66

ECHO

Stress ECHO

Alternative to Myocardial perfusion scanning

Superior to exercise ECG

67

CT Angiography

assessment of symptomatic patients for the

assessment of obstructive disease

higher radiation dosages contraindicate its use as a

screening tool for asymptomatic patients

demonstrate the morphological consequences of

ischemic heart disease

can assess ventricular function and perfusion

visualizing coronary arteries

68

CT Angiography

69

CTA

70

MRA

Assessment of Ventricular volumes, mass, function

Assessment of myocardial infarction and viability

Stress ventriculography

Coronary angiography and flow

Identification of plaque components

Non-invasive and no radiation

Not useful for screening purpose

71

72

Coronary angiography • Provide detailed information

about the extent & nature of

CAD

• Presence of dynamic

coronary vascular lesions,

such as spasm or

thrombosis

• Consequences of CAD, -

IMR or LV dysfunction

• Quantification of severity of

both diastolic and systolic

dysfunction

73

Treatment (Stable Angina)

• Identification and Treatment of Aggravating

Conditions - AV disease, HCM, anemia

• Treatment of Risk Factors – HTN, smoking

• Drug Therapy

• PCI/ CABG

• Enhanced ECP

• Transmyocardial laser revascularization

74

Treatment (Stable Angina) Nitrates

– systemic venodilation, reduction in LV EDV/P,

reducing oxygen requirements; dilation of

epicardial coronary vessels; increased blood flow

in collateral vessels, improve exercise tolerance

– relieve ischemia in UA, Prinzmetal's variant angina

Beta-blockers

- reduce myocardial oxygen demand, inhibiting

increases in heart rate, BP, contractility, esp during

exercise, relief of angina, ischemia

- reduce mortality and reinfarction in patients after

MI

75

Treatment (Stable Angina)

Calcium antagonists

• Coronary vasodilators, variable reductions in

myocardial oxygen demand, contractility, BP

• Indicated when BB contraindicated, poorly tolerated,

ineffective. sick-sinus syndrome, AV conduction

disturbances, symptomatic PAD, Prinzmetal's angina

• Amlodipine and beta blockers have complementary

actions on coronary blood supply and myocardial

oxygen demands.

• Beta blockers have shown to improve life expectancy

following acute MI while CCB have not

76

Treatment (Stable Angina) Aspirin/ Clopidogrel

(ACE) inhibitors - post MI; HTN, chronic IHD,

DM, diabetes, LV dysfunction

Potassium channel activators- nicorandil - open

ATP-sensitive potassium channels in myocytes

Metabolic modulators

Trimetazidine - exert anti-ischaemic properties without

affecting myocardial oxygen consumption and blood

supply, affects myocardial substrate utilization by shifting

energy production from FFA to glucose oxidation.

Ranolazine - symptomatic chronic angina max Rx,

inhibits late inward sodium current (INa)

Perhexiline, etomoxir 77

Treatment Goals

(ACS)

• Restore blood flow to prevent infarct

expansion - STK/ PCI/ CABG

• Prevent death, complications

• Relieve ischemic chest discomfort

• Prevent coronary artery reocclusion

78

Early Pharmacotherapy for ACS

• Intranasal oxygen

• IV NTG - control ischemia

• Morphine

• β-blocker - control ischemia

79

Antiplatelet • Thromboxane A2 inhibitor

-- aspirin

• ADP receptor blockers

– Irreversible (ticlopidine, clopidogrel, prasugrel)

– Reversible (cangrelor)

• Phosphodiesterase inhibitors

– Dipyridamol

– Cilostazol

• Glycoprotein IIb/IIIa antagonists indicated for patients undergoing 1 ˚ PCI in combination with ASA, clopidogrel, & UFH

– Abciximab

– Tirofiban

– Eptifibatide 80

Anticoagulant • UFH

• LMWH (enoxaparin, dalteparin)

• Factor Xa Inhibitor (fondaparinux)

alternative to UFH in patients not undergoing reperfusion

receiving fibrinolytics

not recommended for use alone in 1˚ PCI

• DTI (Lepirudin, Bivalirudin, Argatroban)

option in patients undergoing planned 1˚ PCI

Inhibit clot-bound & circulating thrombin

Antiplatelet activity

• VKA (warfarin)

81

Fibrinolytic

Fibrin non-specific agents

• Streptokinase

• Anistreplase

• Urokinase

Fibrin-specific agents

• rt-PA (alteplase)

• Variants of t-PA

– Substitution (monoteplase, tenecteplase)

– Deletion (reteplase, lanoteplase, pamiteplase)

82

Comparison of Fibrinolytic Agents

Agent Fibrin

Specificity

Complete

Perfusion

at 90

Minutes

Bleeding

risk

Administration

Streptokinase + 35% +++/+ Infusion over 60

minutes

Alteplase +++ 50-60% ++/++ Bolus followed by

infusions over 90

minutes

Reteplase ++ 50-60% ++/++ Two bolus doses, 30

minutes apart

Tenecteplase ++++ 50-60% +/++ Single bolus dose 83

Contraindications to Fibrinolysis

Absolute contraindications

– active internal bleeding (not including menses)

– previous intracranial hemorrhage at any time

– ischemic stroke within 3 months

– intracranial neoplasm

– structural vascular lesion (e.g., AVM)

– suspected aortic dissection

– closed head or facial trauma within 3 months

84

Relative Contraindications – uncontrolled HTN (BP > 180/110 mm Hg)

– ischemic stroke > 3 months

– dementia

– intracranial pathology

– current anticoagulant use

– bleeding diathesis

– traumatic or prolonged CPR (> 10 min)

– major surgery (< 3 wks)

– noncompressible vascular puncture

• recent liver biopsy

• carotid artery puncture

– recent internal bleeding (within 2 to 4 wks)

– previous streptokinase use (> 5 days) or prior allergic reaction

– pregnancy

– active peptic ulcer

– history of severe, chronic, poorly controlled HTN

85

Successful thrombolysis

Clinical

Resolution of chest pain

ECG

> 50 % decrease in max ST elevation at 90

minutes after start of STK

Enzymes

Early peak (3 hrs) of CK-MB

CAG

TIMI III flow

86

PCI

Percutaneous

Coronary

Interventions

Balloons 10%

Stents 80%

Atherectomy 10%

87

PCI As an alternative to thrombolytic therapy in patients with

AMI and STEMI or new or presumed new LBBB who can undergo angioplasty of the infarct artery <12 hr from the onset of ischemic symptoms or >12 hr if symptoms persist, if performed in a timely fashion (performance standard: balloon inflation within 90 ± 30 min of hospital admission) by individuals skilled in the procedure

In patients who are within 36 hr of an acute STEMI/Q wave or new LBBB MI who develop cardiogenic shock, are younger than 75 yr, and revascularization can be performed within 18 hr of the onset of shock by individuals skilled in the procedure

As a reperfusion strategy in candidates who have a C/I to thrombolytic therapy

Objective evidence for recurrent infarction or ischemia

88

PCI Cardiogenic shock or hemodynamic instability

Recurrent angina without objective evidence of ischemia or infarction

Angioplasty of the infarct-related artery stenosis within hours to days (48 hr) following successful thrombolytic therapy in asymptomatic patients without clinical and/or inducible evidence of ischemia

Spontaneous or provocable myocardial ischemia during recovery from infarction

Patients with LV ejection fraction <0.4, CHF, or serious ventricular arrhythmias

All patients after a non-Q-wave MI

89

CABG Surgery reroutes or bypasses blood around clogged arteries

Grafts Arterial - Radial artery, internal mammary artery

Venous – Long saphenous vein

Indications

• Triple vessel disease

• Left Main stem disease

• Failed PCI

• Diffuse disease not amenable to PCI

• Severe LV dysfunction or DM

•Patients with ACS (NSTEMI and STEMI ) need early invasive

strategy

•PCI or CABG depends upon anatomy of vessels and

availability of facilities and expertise 90

PCI vs STK

18TH to 20 th century

Balia district to max saket

• STEMI patients should

receive either fibrinolysis

or primary PCI within 3 hrs

of symptom onset

– PCI: preferred treatment in

capable centers/ high risk

patients/ failed STK

91

Post MI Management • ASA

• Nitrates

• -blocker

• ACE- inhibitors

• Statins

• Aldosterone antagonists/ diuretics

• Anti-coagulation

– large infarcts (especially anterior), CHF, LV

thrombus, DVT, EF< 35 %, AF

Extension / Ischemia

Complications of MI

Acute MI

Arrhythmia

Heart Failure

Expansion / Aneurysm RV Infarct

Pericarditis

Mechanical Mural Thrombus 93

ARRHYTHMIAS

– Most common complication

– PVCs ~ 90%, SVT ~ 10%, CHB ~ 20% RV infarct

– Bradyarrhythmias – common with inferior MI

– Ventricular fibrillation (2-4%)

resuscitation

defibrillation

– Atrial fibrillation

may not require treatment

If hypotension occurs – DC cardioversion

94

Indications for Permanent Pacing

persistent complete (third-degree) AV block

persistent sinus node dysfunction - symptomatic

bradycardia

intermittent second-degree Mobitz II or third-

degree AV block

second-degree Mobitz II or third-degree AV block

with new bundle branch block 95

Extension / Ischemia Post infarct angina – 50%

Inc of CK-MB > 50% than previous nadir

Management same as unstable angina

In distribution of infarct vessel:

IRA reperfusion, then reocclusion

thrombus propogation, distal embolization

At a distance:

reduced collateral flow from IRA

new coronary thrombus

reduced systemic perfusion pressure

increased myocardial oxygen consumption

Treatment:

Pharmacologic (beta blockers, nitrates)

Urgent revascularization

Repeat lytics (antibodies to SK)

96

• Commonly occurs on 2nd -3rd day of infarction

• Results from infarction extending to epicardial

surface of heart, with associated inflammatory

response\

Post MI Syndrome (Dressler’s)

• Fever

• Pericarditis

• Pleurisy

• Weeks to month after infarction

• High dose aspirin or corticosteroids

Pericarditis

97

Right Ventricular Infarction Associated with occlusion of proximal RCA

Classic triad by hypotension, JVP, clear lungs

ECG: ST in RV4

Echo: RV dilation and hypokinesia

Management Usually transient ischemic dysfunction with long-

term recovery common

Marked sensitivity to preload reduction (nitrates)

Fluid volume infusion for hypotension and low

cardiac output

98

Infarct Expansion “ Aneurysm ” Circumscribed non-contractile outpouching of LV

Usually composed of fibrous tissue + necrotic muscle

+/- viable myocardium .

Develops in 8 – 15% of patients post MI

Common after AWMI with totally occluded poorly

collateralized LAD

Rarely seen with multivessel disease

Potential consequences:

Mural thrombus +/- embolization

Adverse LV remodeling and CHF

ventricular rupture

ventricular arrhythmias 99

Differences between a pseudoaneurysm and true aneurysm 100

Infarct Expansion “ Aneurysm ”

101

Heart (LV) failure & shock • Cardiogenic shock:

– 6 % of STEMI, 2 % of NSTE ACS

– Mortality rate: 60%

– LV wall > 40% infarcted

• Diastolic or systolic dysfunction may predominate

.

Extensive LV infarctions

Impaired relaxation, compliance

Extensive RV infarction or ischemia

VSD or acute severe MR

Tamponade (with or without free wall rupture)

Others - sepsis, beta- or Ca+2-blocker overdose,

pulmonary embolism 102

Heart (LV) failure & shock • Correction of hypoxemia, acidosis, bradycardia, AV block,

new onset AF

• Mechanical circulatory support + inotropic support

• Correction of hypoxemia, acidosis, bradycardia, AV block,

new onset AF

• Mechanical circulatory support + inotropic support

• LV and biventricular assistance devices

• Percutaneous cardiopulmonary bypass support

• Intraaortic Balloon Counterpulsation

– Extremely effective in supporting patients

undergoing coronary angiography,

PTCA, and CABG in cardiogenic shock.

– provides bridging support until an LV

assistance device can be implanted or

cardiac transplantation can be performed

103

• Incidence of clinically evident systemic embolism after MI < 2%.

• Increases in patients with AWMI

• Incidence of mural thrombus after MI - 20%

LV thrombus and emboli

• Systemic embolism -10% of LV thrombus

• Risk is highest in the first 10 days but persists at least 3 months

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Mechanical complications

Ventricular septal rupture

2-5 days post MI

Free wall rupture

within 2 weeks post MI

Ischemic MR

13 hours post MI

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Ventricular Septal Rupture

Incidence - 1-3% of transmural Mis

Medical stabilization and IABP

Early surgical repair for decompensated pts

Small asymptomatic VSDs may not require repair

Sudden appearance of loud systolic murmur and

thrill medial to the apex along the left sternal

border in the 3rd or 4th intercostal space,

accompanied by hypotension with or without signs

of LV failure, is characteristic 106

Acute Mitral Regurgitation

Transient MR common in early MI (20-40%)

Persistent MR, even mild, associated with increased long-

term mortality post-MI

Due to papillary muscle or chordal rupture or dilation of

ventricle and annulus

Most common with inferior MI

Early transient late apical systolic murmur thought to

represent papillary muscle ischemia

Sudden hemodynamic deterioration common

Stabilize medically, IABP, then surgical repair 107

Free Wall Rupture

Less frequent (1-3.4%), but earlier with STK

Uncontained sudden death or asystole

Pseudoaneurysm transient hypotension,

bradycardia, repetitive emesis, restlessness

Echocardiogram usually diagnostic

Surgical repair - may require pericardiocentesis for

uncontained rupture

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Post MI Complications “ACT RAPID”

• Arrhythmias

• Congestive Heart Failure

• Tamponade / Thromboembolic disorder

• Rupture (Ventricle, septum, papillary muscle)

• Aneurysm (Ventricle)

• Pericarditis

• Infection

• Death / Dressler’s Syndrome

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PREVENTION PRIMORDIAL

• Preventing spread of CHD risk factors and life

styles that have not yet appeared or become

endemic by Mass education

PRIMARY

• Aims at reversing risk factors that have established

themselves

• Population strategy, High risk strategy

• It includes :- TLS modifications 110

2˚MI Prevention Goals

• Control modifiable CAD risk factors

• Prevent development of systolic HF

• Prevent recurrent MI, stroke

• Prevent death, including SCD

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2˚MI Prevention Drugs

• ASA

• -blocker

• ACE- inhibitors

• Statins

Exercise

Walking, jogging or bike riding

Intensity – 70 – 85% of Heart Rate max

Duration – 30 minutes with warm up 5 minutes and cool

down 5 minutes

Frequency - 5 times a week

Dietary goals

-Fat limited to 20-30% of total daily intake

-Saturated fats upto 10%

-PUFA upto 10%

-Refined carbohydrate

-Protien upto15%

-Fibre upto 20-30mg%

-Cholesterol <200mg%

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17th dynasty princess, “Ahmose-Meryet-Amon"

1550-1580 BCE

Horus Study of Ancient Egyptian Mummies

♂ 33M 40±10.2 y ♀17F 37.6±12 y

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Thank you

Access this powerpoint at

http://dramiteshaggarwal.yolasite.com

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